Related Experiment Video
Updated: Jun 14, 2026
Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
Chrysin alleviates pressure overload-induced myocardial remodeling through regulating the PI3K/AKT/NRF2
Yijia Wang1, Xing Feng1, Shuhui Zhao1
1Basic Medical Research Center, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
Insights
Chrysin (CHR) protects against heart failure by reducing myocardial remodeling, inflammation, and apoptosis. It works by regulating the PI3K/AKT/NRF2 pathway, offering a potential therapeutic for pressure overload-induced cardiac diseases.
Area of Science:
- Cardiology
- Pharmacology
- Molecular Biology
Background:
- Oxidative stress is a key factor in heart failure pathogenesis, driving myocardial remodeling, hypertrophy, and fibrosis.
- Chrysin (CHR) exhibits antioxidant, anti-inflammatory, and anti-apoptotic properties, suggesting therapeutic potential.
Purpose of the Study:
- To investigate Chrysin's protective effects against pressure overload-induced myocardial remodeling.
- To elucidate the underlying molecular mechanisms of Chrysin's action in cardiac dysfunction.
Main Methods:
- Established mouse models of cardiac hypertrophy via transverse aortic constriction (TAC).
- Utilized angiotensin II (Ang II) to induce cardiomyocyte hypertrophy in H9C2 cells.
- Employed bioinformatics analysis and Western blot to explore signaling pathways.
Main Results:
- Chrysin improved survival, cardiac function, and reduced hypertrophy and fibrosis in TAC mice.
- CHR inhibited inflammatory mediators (TNF-α, IL-1β), apoptosis (BAX, Cleaved-Caspase-3), and enhanced anti-apoptotic BCL-2.
- CHR upregulated antioxidant enzymes (SOD1, HO-1) via NRF2 activation, linked to the PI3K/AKT pathway.
Conclusions:
- Chrysin ameliorates pressure overload-induced myocardial remodeling by modulating the PI3K/AKT/NRF2 pathway.
- CHR alleviates oxidative stress, inflammation, and apoptosis in cardiac cells.
- Chrysin shows promise as a therapeutic agent for pressure overload-induced heart diseases.
Background:
Oxidative stress plays a pivotal role in the pathogenesis of heart failure and is closely linked to myocardial remodeling, which includes myocardial hypertrophy and fibrosis. Chrysin (CHR) has multiple medicinal effects such as antioxidant, anti-inflammatory, and anti-apoptosis. This research seeks to investigate whether CHR can protect against pressure overload-induced myocardial remodeling and to explore the underlying mechanism.
Methods:
Transverse aortic constriction (TAC) surgery was conducted to establish a model of cardiac hypertrophy on male C57BL/6J mice. A model of cardiomyocyte hypertrophy in H9C2 cells induced by angiotensin II (Ang II) was also established.
Results:
The results showed that CHR significantly improved survival and cardiac function, reduced myocardial hypertrophy and fibrosis, inhibited the expression of inflammatory mediators TNF-α and IL-1β, suppressed cell apoptosis rate, downregulated the levels of Bcl-2 Associated X protein (BAX) and Cleaved-Caspase-3, and upregulated B-cell lymphoma/leukemia 2 (BCL-2) expression in TAC surgical mice or Ang II-treated H9C2 cells. CHR could also upregulate the levels of antioxidant enzymes SOD1 and HO-1 by mediating the nuclear translocation and expression of NRF2 to counteract oxidative stress response. The further mechanism investigation utilizing bioinformatics analysis and western blot revealed that the disease of heart failure is associated with the phosphatidylinositol‑3‑kinase (PI3K)/serine/threonine-protein kinase B (AKT) signaling pathway.
Conclusions:
Collectively, our findings demonstrated that CHR might exert the improvement effects on pressure overload-induced myocardial remodeling with hypertrophy and fibrosis through regulating the PI3K/AKT/NRF2 pathway-mediated oxidative stress response to alleviate myocardial cell inflammation and apoptosis, suggesting that CHR may be a promising therapeutic agent for cardiac diseases induced by pressure overload.
Related Concept Videos
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
01:26Atherosclerosis III: Management